Chemistry Reference
In-Depth Information
derived from the erroneous idea that the action of lutein was similar to vitamin A in the visual process
(von Studnitz and Loevenich 1947). Lutein at that time was believed to be a precursor of vitamin A like
β
-carotene. Today, however, we know that lutein and zeaxanthin do not have any provitamin A activity
(Weiser and Kormann 1993). Nevertheless, in a substantial number of studies improving effects on dark
adaptation could indeed be demonstrated (Monje 1948, Cüppers and Wagner 1950, Klaes and Riegel
1951, von Studnitz 1952, Andreani and Volpi 1956, Cuccagna 1956, Mosci 1956, Mueller-Limmroth
and Schmidt 1961b, Cilotti 1963), while other authors (Wuestenberg 1951, De Ferreira and Da Maia
1956, Pfeifer 1957) were not able to coni rm these effects. The most frequently used doses ranged from
5 to 20 mg of the ester and were taken over periods of 2-6 weeks. Hayano et al. (1959) appear to have
been the i rst and only scientists who followed adaptinol treatment with measuring plasma concentra-
tions of lutein. They did this i rst in frogs and presented evidence that parenteral administration of
helenien increased its levels in liver and blood. In humans, they found that adaptinol supplementation
increased the lutein plasma level in normal subjects and that dark adaptation improved proportionally.
Interestingly, the plasma lutein levels of patients with retinitis pigmentosa (RP) were initially very
low and clinical improvement in dark adaptation could only be demonstrated in patients who showed
an increase of plasma lutein levels. Adaptinol was also tested in subjects with various other ophthal-
mic diseases, in particular night blindness (Oka 1955, Andreani and Volpi 1956, Cuccagna 1956, De
Ferreira and Da Maia 1956, Mosci 1956, Hayano, Koide et al. 1959, Sole et al. 1984), but also myo-
pia (Asciano and Bellizzi 1974, Sole et al. 1984) and tapeto-retinal degenerations (Mueller-Limmroth
and Kueper 1961a), with mixed results being reported. After 1984, interest in helenien and adaptinol
appears to have vanished as no respective publications can be retrieved after then.
The above-mentioned early supplementation studies with xanthophylls did not measure the
changes in MPOD associated with supplementation probably because an easy-to-use technique for its
noninvasive measurement in the human retina eye was not available at that time. The i rst apparatus
for this purpose had been described in 1953 by deVries et al. (1953) and it is only since the 1970s that
publications can be found that report on systematic measurements of MPOD in the human retina.
13.8.2 L
UTEIN
'
S
AND
Z
EAXANTHIN
'
S
R
OLE
IN
R
ISK
R
EDUCTION
OF
AMD
For hundreds of years, the dried fruit of the Chinese wolfberry (also called
Fructus lycii
), “Gou
Qi Zi” (
Lycium barbarum
) has been a constituent of traditional Chinese herbal medicine for the
treatment of visual disorders (Huang 1993, Benzie et al. 2006). This probably was the i rst recorded
“medicinal use” of one of the macular xanthophylls. The dried fruit contains high levels of zeaxan-
thin-dipalmitate, up to 1.1 g/kg (Inbaraj et al. 2008), making zeaxanthin a logical lead compound
for this plant, which is not only prescribed as a medicine but also commonly used in home cooking
in China. Plasma levels of zeaxanthin increase when ingesting this berry (Breithaupt et al. 2004).
Furthermore, MPOD levels increased signii cantly in 7 volunteers who received daily doses of
about 20 mg zeaxanthin via ingesting this berry for 3 months (Leung et al. 2001).
AMD is, as the name implies, an age-related degenerative condition of the macula. If the macula
becomes dysfunctional, visual tasks requiring high resolution such as recognizing faces or reading
become progressively more difi cult until, in the late stages of advanced AMD, they become impos-
sible. Advanced AMD is the leading cause of legal blindness in the United States and other developed
countries, and it is expected that the prevalence of this disease will drastically increase, and may
reach close to 3 million individuals within less than 20 years in the United States alone (Friedman
et al. 2004). Evidence of AMD is i rst observable for most individuals between the ages of 55 and 65
with the build up of characteristic yellow deposits within and around the macular area. These depos-
its, called drusen, contain lipofuscin and its derivatives. Most people with these early changes still
have satisfactory vision but they are at risk of developing advanced AMD. Advanced AMD, which
is responsible for profound vision loss, has two forms: dry and wet. Central geographic atrophy,
the “dry” form of advanced AMD, causes these problems through loss of photoreceptors and cells
supporting the photoreceptors in the central part of the retina. Currently, no treatment is available for
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